Disorders that result in hyperproliferation of the epidermis such as corns, calluses, keratosis pilaris, psoriasis, and other less common conditions, account for a large percentage of skin disease worldwide. A commonality among these disorders is that friction and/or pressure typically precipitate or worsen the clinical manifestations of the disease. The shared molecular feature among these disorders of hyperproliferation is expression of a panel of keratins (the hyperproliferation keratins, K6, K16, and K17).
Keratosis pilaris is a very common, benign skin condition in which keratin protein in the skin forms hard plugs within hair follicles and often lessens or disappears with age. KP consists of a clustering of small, usually 1-2 mm, flesh-colored to slightly erythematous follicular bumps commonly found on the backs of the upper arms. The texture is frequently very coarse due to protrusion of the keratin plugs from the hair follicles. KP may also appear on the buttocks and thighs, where it may be precipitated or worsened by friction from clothing. Less commonly, KP can be seen on the face, where it is termed KP atrophicans faciei. Histologically, these lesions demonstrate keratin plugging of the hair follicles. The condition is generally worse in winter and may improve in the summer. It is associated with atopic dermatitis (eczema) and is hereditary, but the genetic basis of the disease is unknown.
Indeed, the underlying genetic cause of corns, calluses, and psoriasis also remains unknown, but they are similarly caused by friction and pressure generated between the foot and footwear. Histologically, these lesions show a thickened stratum corneum and over time, they develop a central keratin plug that presses painfully into the dermis. The shared pathophysiology involved in the development of corns, calluses, and KP lesions likely explains the shared overexpression of the hyperproliferative keratins.
Psoriasis, although not considered to be a classic disorder of keratinization, also shows overexpression of the hyperproliferative keratins, primarily K16 and K17. In addition, psoriatic lesions tend to develop or extend into areas of trauma, where these same keratins are activated (a symptom referred to as Koebnerization).
Although good emollients or topical treatment with keratolytic agents such as urea, lactic acid, Retin A (tretinoin), or vitamin D analogs may soften and soothe the symptoms of epidermal proliferation, there is currently no medication that eliminates the disease manifestations. Available treatments are directed at symptomatic manifestations of the disorders but generally do not affect the underlying cause as it has heretofore been unknown. As individual patients are generally troubled by different manifestations of the disease, no single treatment plan is known to be effective for treating the hyperproliferation as a whole. Treatment options for epidermal hyperproliferation fall into several broad categories, non-invasive (mechanical), invasive (surgical), chemical, and pharmacological. Currently no treatment options are available for corns, calluses or KP, which address the underlying cause of the disorder and therefore prevent the occurrence of symptoms.